Comparison of micro- and macrovascular endothelial cells (brec and
baec) in [beta]-adrenergic regulation of transendothelial
permeability.
Zink, Sigrid, Peter R[diaeresis]osen, and Horst Lemoine.
R[diaeresis]osen, P. und S. Zink Diabetes-Forschungsinstitut,
D[umlaut]usseldorf, Germany, Lemoine, H., Institut f[umlaut]ur
Lasermedizin, Heinrich-Heine-Universit[umlaut]at D[umlaut]usseldorf,
D[umlaut]usseldorf, Germany
APStracts 2:0214C, 1995.
Barrier function of EC was modulated using [beta]-adrenergic agonists
e.g. isoproterenol (ISO) and formoterol (FOR). To get a direct
comparison between EC from different vascular sources, we isolated
cells from aorta (BAEC) and retina (BREC) of the same calf. For
permeability studies, EC were cultured on polycarbonate filters. At
confluency, transendothelial exchange (TEE) of the diffusion marker
FITC-dextran was determined. Microvascular, retinal EC monolayers are
half as permeable as monolayers from macrovascular BAEC. Stimulated
with [beta]AR-agonists, monolayer-permeability decreases and the
amount of intracellular cAMP increases in both cell-types. Comparison
of the half-maximum reactions (pEC50) shows direct coupling between
[beta]AR and AC: The [beta]2-selective agonist FOR stimulates cAMP
synthesis in BAEC with pEC50=9.37 and decreases permeability with
pEC50=9.72. In BREC the pEC50's of ISO concerning stimulation of cAMP
synthesis and the decrease of permeability are also very similar:
5.32 and 5.34. BREC are not as sensitive to [beta]2-agonists as BAEC.
The pEC50 of FOR-influence on BREC permeability is 8.77 in comparison
to 9.72 for BAEC. These results could be interpreted with different
affinities of the [beta]2-selective AR in BREC and BAEC.
Received 3 January 1995; accepted in final form 3 May 1995.
APS Manuscript Number C2-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 May 1995.